Clostridium botulinum toxin

Clonal Selection Clostridial Neurotoxins Clostridium Botulinum Toxin Clotting CNTF... 

Delayed-action paralytic neurotoxins that block the release of acetylcholine causing a symmetric, descending flaccid paralysis of motor and autonomic nerves. Paralysis always begins with the cranial nerves. Toxins are obtained from an anaerobic bacteria (Clostridium botulinum). Toxin A is a white powder or crystalline solid that is readily soluble in water. It is stable for up to 7 days as an aqueous solution. All toxins are destroyed by heat and decompose when exposed to air for more than 12 h. 

Bose-Einstein condensation, 17 352 Bosons, 17 352 Boswellic acids, 24 557 Botox (Clostridium botulinum toxin type A), 2 816 Bottle centrifuge operation, 5 528-529 theory of performance, 5 507-508 Bottle polymerizatioi, 20 376 Bottles... 

Clostridium botulinum (Type A-Str.62), exposure to ethylene-dichlorodifluoro-methane mixture, 8 635t Clostridium botulinum toxin (Botox) type A, 2 816... 

The binary Clostridium botulinum toxin C2 blocks the function of actin filaments similarly to cytochalasin D (92). Treatment is for one to four hours in concentrations of 50ng/100ng or 100ng/200ng prior to adding liposomes. 

McGrath, S., Dolley, J.S.G. and Haylock, R.W., Quantification of Clostridium botulinum toxin gene expression by competitive reverse transcription PCR, Appl. Env. Microbiol., 66, 1423-1428, 2000. 

Powder for injection (vacuum-dried) 100 units of vacuum-dried Clostridium botulinum toxin type A neurotoxin complex- (Rx)... 

Ogert, R. A., Brown, J. E., Singh, B. R., Shriver-Lake, L. C., and Ligler, F. S. (1992). Detection of Clostridium botulinum toxin A using a fiber optic-based biosensor. Ami. Biochem. 205, 306-312. 

The complex of SNAREs and SNAP25 is the target of the powerful Clostridium, botulinum, toxin, a protease that cleaves specific bonds in these proteins, preventing neurotransmission and causing the death of the organism. Because of its very high specificity for these proteins, purified botulinum toxin has served as a powerful tool for dissecting the mechanism of neurotransmitter release in vivo and in vitro. 

Botulism A (Clostridium botulinum toxin) Bacteria— food (particularly improperly canned foods), wound, and infantile 1-5 days No Standard Descending muscle paralysis, ptosis (drooping upper eyelids), blurred vision/ diplopia Fatal about 4-6 days nonfatal several months Aggressive resp support, supportive care trivalent and heptavalent antitoxin... 

O Sullivan G, Mohammed N, Foran P, Lawrence G, Dolly O (1999) Rescue of exocytosis in botulinum toxin A-poisoned chromaffin cells by expression of cleavage-resistant SNAP-25. Identification of the minimal essential C-terminal residues. J Biol Chem 274 36897-904 Oberg SG, Kelly RB (1976) The mechanism of beta-bungarotoxin action. I. modification of transmitter release at the neuromuscular junction. J Neurobiol 7 129 11 Ohishi I, Sugii S, Sakaguchi G (1977) Oral toxicities of Clostridium botulinum toxins in response to molecular size. Infect Immun 16 107-9... 

Sakaguchi G (1982) Clostridium botulinum toxins. Pharmacol Ther 19 165-94 Sankhla C, Jankovic J, Duane D (1998) Variability of the immunologic and clinical response in dystonic patients immunoresistant to botulinum toxin injections. Mov Disord 13 150-54 Schantz EJ, Johnson EA (1997) Botulinum toxin the story of its development for the treatment of human disease. Perspect Biol Med 40 317-27 Schiavo G (2006) Structural biology dangerous liaisons on neurons. Nature 444 1019-20 Schiavo G, Matteoli M, Montecucco C (2000) Neurotoxins affecting neuroexocytosis. Physiol Rev 80 717-66... 

Coleman, I. (1954). Studies on the oral toxicity of Clostridium botulinum toxin, type A. Can J. Biochem. Physiol. 32 27-34. 

Iakovlev, A. (1958). The importance of antitoxic immunity for the defence of the body in respiratory penetration by bacterial toxins. I. Role of passive immunity in the defence of the body against respiratory disease caused by Clostridium botulinum toxins. J. Microbiol. Epidemiol. Immunobiol. 29 904-9. 

Ohishi, I., Sugii, S., Sakaguchi, G. (1977). Oral toxicities of Clostridium botulinum toxins in response to molecular size. Infect. Immun. 16 107-9. 

Nemroinuscular blocking agents used in clinical practice interfere with this process. Natural substances that prevent the release of acetylcholine at nerve endings exist, e.g. Clostridium botulinum toxin (see p. 429) and some venoms. 

Hambleton P. Clostridium botulinum toxins a general review of involvement in disease, structure, mode of action and preparation for clinical use. J Neurol 1992 239(l) 16-20. 

Ambache, N. 1951. A further survey of the action of Clostridium botulinum toxin upon different type of autonomic nerve Hbre. J. Physiol. (London), 113 1-17. 

Sakaguchi, G. 1982. Clostridium botulinum toxins. Pharmacol. Ther. 19 165-194. 

Santos, J.l., Swensen, P., and Glasgow, L.A. 1981. Potentiation of Clostridium botulinum toxin aminoglycoside antibiotics chnical and laboratory observations. Pediatrics 68 50-54. 

Figure 5a. Dose/response curves of best fit in the observed range for mouse deaths from Clostridium botulinum toxin. (Gamma and Armitage-Doll models too close to Weibull to distinguish.)...

Figure 5b. Projection of dose/response curves for Clostridium botulinum toxin to region of low dose.

Rivera, V.R., Gamez, F.J., Keener, W.K., White, J.A., and Poli, M.A. (2006) Rapid detection of Clostridium botulinum toxins A, B, E, and F in clinical samples, selected food matrices, and buffer using paramagnetic bead based electrochemiluminescence detec tion. Analytical Biochemistry, 353, 248 256. 

Botulism — Clostridium botulinum toxin is composed of polypeptides or proteins designated A throngh G with molecular weights of 200,000 to... 

Fig. 9.5.6 Direct detection and amplification of the protein toxin Clostridium botulinum toxin A (toxoid). The upper line is an average of three channels with ant -botulinum antibody on the surface.

The release of ACh and other neurotransmitters by exocytosis is inhibited by botulinum and tetanus toxins from Clostridium. Botulinum toxin acts in the nerve ending to reduce ACh vesicular release (see Chapters 9 and 63 for therapeutic uses of botulinum toxin). 

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